Evidence for a cross-talk between human neutrophils and Th17 cells.

By M. Pelletier, L. Maggi, A. Micheletti, E. Lazzeri, NICOLA TAMASSIA, C. Costantini, L. Cosmi, C. Lunardi, F. Annunziato, S. Romagnani and 1 more. Blood, 2010

798 citations recorded by the source corpus.

Interleukin-17A (IL-17A) and IL-17F are 2 of several cytokines produced by T helper 17 cells (Th17), which are able to indirectly induce the recruitment of neutrophils. Recently, human Th17 cells have been phenotypically characterized and shown to express discrete chemokine receptors, including CCR2 and CCR6. Herein, we show that highly purified neutrophils cultured with interferon-gamma plus lipopolysaccharide produce the CCL2 and CCL20 chemokines, the known ligands of CCR2 and CCR6, respectively. Accordingly, supernatants from activated neutrophils induced chemotaxis of Th17 cells, which was greatly suppressed by anti-CCL20 and anti-CCL2 antibodies. We also discovered that activated Th17 cells could directly chemoattract neutrophils via the release of biologically active CXCL8. Consistent with this reciprocal recruitment, neutrophils and Th17 cells were found in gut tissue from Crohn disease and synovial fluid from rheumatoid arthritis patients. Finally, we report that, although human Th17 cells can directly interact with freshly isolated or preactivated neutrophils via granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and interferon-gamma release, these latter cells cannot be activated by IL-17A and IL-17F, because of their lack of IL-17RC expression. Collectively, our results reveal a novel chemokine-dependent reciprocal cross-talk between neutrophils and Th17 cells, which may represent a useful target for the treatment of chronic inflammatory diseases.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/b887eb9719fe56554fc67681d69e250491f22385

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Citations in the corpus

Neutrophil: A Cell with Many Roles in Inflammation or Several Cell Types? (2018, background): “In turn, Th17 cells recruit more neutrophils (Pelletier et al., 2010; Zenobia and Hajishengallis, 2015).”
Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis. (2011, background): “, defensins, lipocalin, and S100 proteins) and also regulates a group of neutrophil-attracting CXCL chemokines (Nograles et al., 2008; Harper et al., 2009; Pelletier et al., 2010).”
Neutrophil-Derived Cytokines: Facts Beyond Expression (2014, background): “However, since the data on the effective capacity of human neutrophils to express/produce IL-17 (11, 50) or IFNγ (51, 52) are still controversial in literature, we can only report on studies carried out in mice.”
Neutrophil cell surface receptors and their intracellular signal transduction pathways (2013, background): “The NLRP3 inflammasome processes p (primarily IL-17A and IL-17F), neutrophils do not express IL-17 receptors and do not respond to IL-17 directly [177].”
Phagocyte partnership during the onset and resolution of inflammation (2010, background): “It has also been described that neutrophils can express CCL20 when exposed to pro-inflammatory stimuli such as TN”
Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “Neutrophils, in turn, recruit Th17 cells via release of the chemokines CCL20 and CCL2, resulting in a positive feedback loop between neutrophils and Th17 cells [103].”